There is a serious problem with the way evangelical
scientists view evolution. For example, the "Call for Papers: 1994 Annual
Meeting Symposium" asks "whether the scientific data justify
extrapolating from microevolutionary changes produced by natural selection to
the production of new body plans and
structures."1 The answer must be
"No," for the question prejudges the
problem.2 The first difficulty is that natural
selection does not produce microevolutionary changes. It does not, indeed
cannot, drive mutations. It merely sorts among such mutations as they
occur.3

The introductory question of the call is broader: "Is
the neo-Darwinian mechanism of selection of random mutations adequate for the
creation of major biological innovations?" The answer is still
"No." The accumulation of mutations, translocations, transpositions,
and inversions seems to produce "good" species within genera or
families. The Hawaiian Drosophila come immediately to mind. Ecological
niches occupied and behavioral changes in timing and mating signals prevent
interbreeding in the wild.4 Genetic modifications
affect, and even control, all these. But no accumulation of mutations in the
small genome of an entity like a dipteran can produce the large genome of a
vertebrate. Also, any radical change in an essential gene will almost certainly
reduce viability. It may well be lethal.

A First Look: Color

If we step back from a simple consideration of mutations, we
may ask whether there is any way in which a vital gene can take on new functions
without sacrificing the old.5 The answer appears
to be "Yes." A crude example occurs in color vision. Human beings,
like many other mammals, have genes for color vision on different chromosomes.
The visual pigment giving blue sensitivity is produced by a gene on an autosome.
The two visual pigments giving green and red sensitivity are produced by genes
on X, the sex chromosome.6 This is why
color-blindness is thought of as a sex-linked recessive. Both genes on X are
very similar. The visual pigments for which they code are just different enough
to shift their peak spectral absorption somewhat. This shifting produces very
subtle differences in color vision.7 The pigment
giving blue sensitivity is also similar, as is rhodopsin, which gives the rods
monochromatic sensitivity. Fish produce rhodopsin. Blue vision is widespread
among mammals. American monkeys have a gene for red visual pigment on the sex
chromosome. Chimpanzees add green visual pigment. The simplest biological
explanation for these phenomena is that the original rhodopsin gene was
duplicated and the replication mutated. This produced the continued ability to
see plus the new ability to differentiate some colors in bright light. Later, a
similar process produced the added ability to detect red, giving enhanced color
discrimination. Finally, the new ability to see green produced full trichromatic
vision.8 At each stage, enhanced sensitivity would
plausibly be selected for, whereas modification of the original genes without
duplication would surely be deleterious, except perhaps for creatures like blind
cave fish. There is another piece of evidence that bolsters this explanation:
some human X-chromosomes carry more than one copy of the gene for green visual
pigment.9 Those with this unusual genotype have a
normal phenotype.

One may also ask whether an organism can acquire new genes
from outside the species. The answer appears to be "Yes." Germs are
known to transfer resistance to antibiotics from one bacterial species to
another. Some viruses transfer genetic material between plants. More recently,
evidence has been found that transfer by arthropods can occur among insects. So
viruses, bacteria and small arthropods are potential
vectors.10

The Genetic Attic

Recent evidence shows that a duplicated gene may become
quiescent rather than taking on new duties. Researchers found a gene that they
estimate has not been active for about five million years in the mouse
genome.11 This gives additional support to the
view that the large mammalian genome results from the accumulation of duplicate
DNA. Some of this may be currently without function, "junk DNA."
However, I keep reading of functions, especially control functions, discovered
for some introns which had been written off as
"junk."12 The most surprising
development to me is that a functional coding sequence may be embedded in an
intron.13 This brings to mind the long list of
vestigial organs once given,14 at least mainly the
product of ignorance of the endocrine system. So it behooves us to say only that
parts of the genome are currently without known function, rather than declaring
them without function. Unfortunately, where careful scientists insert
qualifications, popular and semi-popular reports often omit them.

Managing Structure: Homologies

Scientists long ago observed that embryos
develop in an orderly fashion. More recently they have discovered that aspects
of the progression are controlled by strings of genes called homeoboxes. The
nature and distribution of these control sequences also bear on the possibility
that reduplication and modification of genes may produce radically different
body plans and structures. A relatively small number of homeobox genes were
found to lie sequentially on a Drosophila chromosome. During
embryogenesis, they were activated sequentially to control the development of
segments on the cephalo-caudal axis. Mutations of these genes produce leg-like
structures in place of antennae, four wings in place of the normal two wings and
halteres, or embryonic death.

Using probes derived from Drosophila genes,
geneticists have discovered a much larger number of mammalian homeobox genes.
They function like the dipteran genes, although the radically different body
plans necessarily produce clearly different effects. A fruit fly, larva or
adult, has clearly delimited segments whose sequential development can be tied
directly to specific homeoboxes. A mammalian embryo has a much more complex
pattern of development, requiring more than one sequence. Nevertheless, it
appears that strings of such genes are activated sequentially to control the
various stages of development. Further, the Drosophila sequence and the
several mammalian sequences are clearly similar.15

A different type of control gene contains a sequence of
thymine and adenine residues (abbreviated as T and A), whose duplication
produces the name, TATA-boxes. These genes are even more broadly
conserved.16 Apoptosis is controlled by similar
genes in Drosophila and Xenopus.17
The list may be extended by those familiar with the literature, for 40% of the
genes are homologous in Drosophila and Homo.18

Obviously, the total embryonic environment has much to do
with the effect of any gene. There is no way that the gene controlling
production of legs, wings, and halteres on the three segments that fuse to form
the insect thorax can trigger similar organs in a chordate, let alone a mammal.
Further, as scientists gain more understanding of the work of control genes,
they find them acting in more complex ways, being reactivated a second time
during development, or even apparently having a function in the adult
organism.19 Despite all these complexities of
function, it has been shown that a mammalian gene can replace a defective
dipteran gene, and even a yeast gene. Apparently, the structure of some vital
genes has been conserved while duplicated genes have mutated, combined, or
otherwise changed to take on different functions.

Bumps Under The Carpet

Besides gene duplication and mutation, there are additional
possibilities for change. Polyploidy, hybridization, chromosome breakage and
recombination, reassortment of introns and exons within and among genes,
including transpositions and inversions, along with position effects, may
combine to effect more radical changes than most of us expect. I have not
encountered any indication that we have deciphered the factors that
differentiate the relatively simple segmentation of annelids from the more
complex patterns of arthropods, or the gene-activation pattern transforming the
bilateral embryonic body into a radially organized starfish or sea urchin. Until
all such matters have been deciphered and it can be shown that no genetic
process can connect one pattern of development to another, we must not claim
that evolutionary descent is impossible. To suggest that evolution is not
reasonable because simple mutation cannot produce the required changes, is to
bear false witness.

Where Next

Do these considerations show that an updated neo-Darwinian
mechanism has provided an adequate explanation for the development of radial,
externally supported and internally supported animals from a single aboriginal
form? No. Do they suggest experiments to transform "primitive" animals
into "advanced" forms? No, for all are, ex hypothesi, the
latest result of eons of modification and
selection.20 But they definitely narrow the gap
between some diverse structures. Also, they suggest the kind of information
which may narrow the gap even more. They clearly need to be faced by honest
investigators.21

2I have assumed
that the scientist is fully open to evidence that macroevolution may have
occurred and is unwilling to bias the investigation. However, the question is
purely rhetorical to some, for they are certain that macroevolution has not, or
cannot, occur. Both 144-hour Creationists and those who believe that the
geologic eras saw multiple creations that suffered only microevolutionary change
fall here. The adherent to dogmatic evolutionism is oppositely biased. I thank
the anonymous referee for calling my attention to this matter.

Samuel L. Scheiner, in his review of Stephen
C. Stearns, The Evolution of Life Histories, notes the broad range of
matters which require consideration in the evaluation of scientific theories of
descent. See Science 258 (11 December 1992): 1820-1822.

8See Maureen
Neitz, Jay Neitz and Gerald H. Jacobs, "Spectral Tuning of Pigments
Underlying Red-Green Color Vision," Science 252 (17 May 1991):
971-974. South American monkeys have a single X-linked pigment apiece which is,
in the species examined, from 96% to 98% identical to the human red pigment.

20Population
genetics adds further complexity by warning us that selection is not simple.
Specialists in various fields will surely add to the list of relevant
considerations.

21Stephen C.
Meyer (Symposium, ASA Annual Meeting, August 9, 1993) implicitly made a point
that all should remember: evolutionary descent does not preclude design.
Alternatively phrased, a mechanism does not have to be mechanistic,
naturalistic, and materialistic.